Thanks for the input!

I believe N6 binds to HIV’s GP120 protein, not the CD4 receptor, but perhaps it could be both.

I agree about the need to target the appropriate t-cells. My gut feeling is that the reaction was from imperfect antibodies being produced in the fat cells. A step that allows the plasmid to target t-cells will hopefully be formulated for the next iteration.

Regarding the length of the treatment… yeah, I agree, progenitor cells would be a better target but I don’t think it’s necessary to go for stem cells. My associates have been working on this plasmid design, and even if they only get it to last a year, it could be a huge step up for treating/preventing a number of viruses for which treatment has remained elusive.

Regarding skipping steps… yes and no. Being able to prove the concept in humans can save an immense amount of time and money; sparing the need to subject rodents to studies that are ultimately pointless. If patients, for whom conventional medicine does not work, are willing to try stuff out… the problem is, how do we gain from their experiences? How do we know if something actually worked when n=1; or had horrible side effects, that the pharma company wants to sweep under the rug? … This is not a trivial problem but my next articles address these questions

That all being said, after proving the concept, I agree that pursuing animal studies is the prudent next step before proceeding with clinical trials.